Genes and Nutrition最新文献

{"title":"A double knockout for zinc transporter 8 and somatostatin in mice reveals their distinct roles in regulation of insulin secretion and obesity.","authors":"Zhongyue Yang, Catherine P Kirschke, Yimeng Cai, Liping Huang","doi":"10.1186/s12263-024-00759-0","DOIUrl":"10.1186/s12263-024-00759-0","url":null,"abstract":"<p><strong>Background: </strong>Both zinc transporter 8 (ZnT8) and somatostatin (Sst) play crucial roles in the regulation of insulin and glucagon secretion. However, the interaction between them in controlling glucose metabolism was not well understood. The aim of this study was to explore the interactive effects of a double knockout of Znt8 and Sst on insulin and glucose metabolism in mice.</p><p><strong>Methods: </strong>Co-expression of ZnT8 with hormones secreted from gastrointestinal endocrine cells of mice was determined using immunofluorescence. Male Znt8 knockout (Znt8KO), Sst knockout (SstKO), double knockout for Sst and Znt8 (DKO), and the wild-type (WT) mice were fed a regular chow diet (CD) or a high-fat diet (HFD) at 3 weeks old for 15 weeks. Weights and fasting or fed glucose levels were determined. Glucose and insulin tolerance tests were performed; metabolic-relevant hormone levels including insulin, glucagon, glucagon-like peptide 1, Pyy, and leptin were determined.</p><p><strong>Results: </strong>ZnT8 is co-expressed with Sst in a subpopulation of endocrine D cells in the gastrointestinal tract. The absence of ZnT8 expression resulted in an increased density of the dense cores in the secretory granules of the D cell. DKO mice had reduced weight compared to WT when maintained on the CD. Compared to Znt8KO and SstKO, DKO mice did not show significant differences in fed or fasting blood glucose level regardless of dietary conditions. However, the CD-fed DKO mice had impaired insulin secretion without alterations in islet morphology or numbers. Moreover, DKO mice displayed diet-induced insulin resistance and disrupted secretion of metabolic-related hormones.</p><p><strong>Conclusions: </strong>Somatostatin as well as a normal insulin sensitivity are required for normalizing glucose metabolism in Znt8KO mice. ZnT8 may play a role in regulating fat mass and leptin secretion. These findings shed light on the multifaceted nature of Znt8 and Sst interactions, opening new avenues to understand their roles in controlling glucose metabolism and fat mass.</p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":"19 1","pages":"24"},"PeriodicalIF":3.3,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11580226/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142683364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genistein inhibited endocytosis and fibrogenesis in keloid via CTGF signaling pathways.","authors":"Chun-Te Lu, Jiunn-Liang Ko, Chu-Chyn Ou, Chih-Ting Hsu, Yu-Ping Hsiao, Sheau-Chung Tang","doi":"10.1186/s12263-024-00758-1","DOIUrl":"10.1186/s12263-024-00758-1","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to evaluate soy isoflavones' effect and potential use-specifically genistein-in treating human keloid fibroblast cells (KFs) and in a keloid tissue culture model.</p><p><strong>Methods: </strong>To investigate the effects of genistein on keloid, a wound-healing assay was performed to detect cell migration. Flow cytometry was used to measure apoptosis. Western blotting and immunofluorescence staining were performed to detect the expression of target proteins. KF tissues were isolated, cultured, and divided into the control, silenced connective tissue growth factor (CTGF) proteins, and shNC (negative control) groups.</p><p><strong>Results: </strong>Genistein suppressed cell proliferation and migration, triggering the cell cycle at the G2/M phase and increasing the expression of p53 dose-dependent in keloids. Genistein inhibited the expression of COL1A1, FN, and CTGF mRNA and protein. Knockdown CTGF reduced the migrated ability in KFs. Genistein also abated TGF-β1-induced keloid fibrosis through the endocytosis model. Separated and cultured the keloid patient's tissues decreased the cell migration ability by genistein treatment and was time-dose dependent.</p><p><strong>Conclusions: </strong>This study indicated that genistein-induced p53 undergoes cell cycle arrest via the CTGF pathway-inhibited keloid cultured cells, and genistein suppressed the primary keloid cell migration, suggesting that our research provides a new strategy for developing drugs for treating keloids.</p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":"19 1","pages":"23"},"PeriodicalIF":3.3,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11520065/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142513327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quercetin supplementation in metabolic syndrome: nutrigenetic interactions with the Zbtb16 gene variant in rodent models.","authors":"Adéla Kábelová, Hana Malínská, Irena Marková, Martina Hüttl, František Liška, Blanka Chylíková, Ondřej Šeda","doi":"10.1186/s12263-024-00757-2","DOIUrl":"10.1186/s12263-024-00757-2","url":null,"abstract":"<p><strong>Background: </strong>Quercetin is a promising phytochemical in treating abnormalities associated with metabolic syndrome (MetS). This study aimed to explore the morphometric, metabolic, transcriptomic, and nutrigenetic responses to quercetin supplementation using two genetically distinct MetS models that only differ in the variant of the MetS-related Zbtb16 gene (Zinc Finger And BTB Domain Containing 16).</p><p><strong>Results: </strong>Quercetin supplementation led to a significant reduction in the relative weight of retroperitoneal adipose tissue in both investigated strains. A decrease in visceral (epididymal) fat mass, accompanied by an increase in brown fat mass after quercetin treatment, was observed exclusively in the SHR strain. While the levels of serum triglycerides decreased within both strains, the free fatty acids levels decreased in SHR-Zbtb16-Q rats only. The total serum cholesterol levels were not affected by quercetin in either of the two tested strains. While there were no significant changes in brown adipose tissue transcriptome, quercetin supplementation led to a pronounced gene expression shift in white retroperitoneal adipose tissue, particularly in SHR-Zbtb16-Q.</p><p><strong>Conclusion: </strong>Quercetin administration ameliorates certain MetS-related features; however, the efficacy of the treatment exhibits subtle variations depending on the specific variant of the Zbtb16 gene.</p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":"19 1","pages":"22"},"PeriodicalIF":3.3,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11515271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142513328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypothetical proteins of chicken-isolated Limosilactobacillus reuteri subjected to in silico analyses induce IL-2 and IL-10.","authors":"Isaac Oluseun Adejumo","doi":"10.1186/s12263-024-00755-4","DOIUrl":"https://doi.org/10.1186/s12263-024-00755-4","url":null,"abstract":"<p><p>Lactic acid bacteria (LAB) probiotics are health-promoting but their characteristics, safety profile and functional mechanisms are not fully understood. Hence, this study aimed to characterize some hypothetical proteins of the chicken-isolated Limosilactobacillus reuteri genome and unravel their IL-2 and IL-10-inducing potential to understand mechanisms of their immunological functionality for sustainable applications. The selected proteins were subjected to in silico analyses for transmembrane topology, sub-cellular localization, IL-2 and IL-10-inducing ability and IL-2 and IL-10 gene expression across various conditions. IL-2 and IL-10-inducing mutants were statistically analyzed using a one-way analysis of variance of a general linear model of SAS and statistical significance was set at p < 0.05. The analyzed proteins are stable under a wide temperature range. All the hypothetical proteins are IL-2 and IL-10-inducing but QHPv.2.12, QHPv.2.13 and QHPv.2.15 are non-immunogenic. The evaluated mutants are IL-2 and IL-10-inducers but QHPv.2.13 and QHPv.2.15 are not immunogenic. This study sheds light on understanding the functional mechanisms of chicken-isolated L. reuteri and suggests it or its proteins as potent candidates for feed additive and therapeutic purposes.</p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":"19 1","pages":"21"},"PeriodicalIF":3.3,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11490116/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142481367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Visnagin alleviates rheumatoid arthritis via its potential inhibitory impact on malate dehydrogenase enzyme: in silico, in vitro, and in vivo studies.","authors":"Abeer A Khamis, Amira H Sharshar, Tarek M Mohamed, Elsayed A Abdelrasoul, Maha M Salem","doi":"10.1186/s12263-024-00756-3","DOIUrl":"10.1186/s12263-024-00756-3","url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disorder. The present study aimed to evaluate the in silico, in vitro, and in vivo inhibitory effect of visnagin on malate dehydrogenase activity and elucidate its inflammatory efficacy when combined with methotrexate in the RA rat model. The molecular docking, ADMET simulations, MDH activity, expression, and X-ray imaging were detected. Moreover, CRP, RF, (anti-CCP) antibody, (TNF-α), (IL-6), (IL-17), and (IL-10) were evaluated. The expression levels of MMP3 and FOXP3 genes and CD4, CD25, and CD127 protein levels were assessed. Histological assessment of ankle joints was evaluated. The results revealed that visnagin showed reversible competitive inhibition on MDH with inhibitory constant (Ki) equal to 141 mM with theoretical IC50 equal to 1202.7 mM, LD50 equal to 155.39 mg/kg, and LD25 equal to 77.69 mg/kg. In vivo studies indicated that visnagin exhibited anti-inflammatory effects through decreasing MDH1 activity and expression and induced proliferation of anti-inflammatory CD4⁺CD25⁺FOXP3 regulatory T cells with increasing the anti-inflammatory cytokine IL-10 levels. Moreover, visnagin reduced the levels of inflammatory cytokines and the immuno-markers. Our findings elucidate that visnagin exhibits an anti-inflammatory impact against RA through its ability to inhibit the MDH1 enzyme, improve methotrexate efficacy, and reduce oxidative stress.</p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":"19 1","pages":"20"},"PeriodicalIF":3.3,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11465529/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142402057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of the oral administration of glycosaminoglycans with or without native type II collagen on the articular cartilage transcriptome in an osteoarthritic-induced rabbit model.","authors":"Roger Mariné-Casadó, Cristina Domenech-Coca, Salvador Fernández, Andrea Costa, Sergi Segarra, Maria José López-Andreo, Francesc Puiggròs, José Joaquín Cerón, Daniel Martínez-Puig, Carme Soler, Vicente Sifre, Claudio Iván Serra, Antoni Caimari","doi":"10.1186/s12263-024-00749-2","DOIUrl":"10.1186/s12263-024-00749-2","url":null,"abstract":"<p><strong>Background: </strong>In a previous study, the 84-day administration of glycosaminoglycans (GAGs), with or without native collagen type II (NC), in an osteoarthritis (OA)-induced rabbit model slowed down OA progression, improved several micro- and macroscopic parameters and magnetic resonance imaging (MRI) biomarkers in cartilage, and increased hyaluronic acid levels in synovial fluid. To elucidate the potential underlying mechanisms, a transcriptomics approach was conducted using medial femoral condyle and trochlea samples.</p><p><strong>Results: </strong>The administration of chondroitin sulfate (CS), glucosamine hydrochloride (GlHCl), and hyaluronic acid (HA), with (CGH-NC) or without (CGH) NC, strongly modulated several genes involved in chondrocyte extracellular matrix (ECM) remodeling and homeostasis when compared to non-treated rabbits (CTR group). Notably, both treatments shared the main mechanism of action, which was related to ECM modulation through the down-regulation of genes encoding proteolytic enzymes, such as ADAM metallopeptidase with thrombospondin type 1 motif, 9 (Adamts9), and the overexpression of genes with a relevant role in the synthesis of ECM components, such as aggrecan (Acan) in both CGH-NC and CGH groups, and fibronectin 1 (Fn1) and collagen type II, alpha 1 (Col2A1) in the CGH group. Furthermore, there was a significant modulation at the gene expression level of the mTOR signaling pathway, which is associated with the regulation of the synthesis of ECM proteolytic enzymes, only in CGH-NC-supplemented rabbits. This modulation could account for the better outcomes concerning the microscopic and macroscopic evaluations reported in these animals.</p><p><strong>Conclusions: </strong>In conclusion, the expression of key genes involved in chondrocyte ECM remodeling and homeostasis was significantly modulated in rabbits in response to both CGH and CGH-NC treatments, which would partly explain the mechanisms by which these therapies exert beneficial effects against OA.</p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":"19 1","pages":"19"},"PeriodicalIF":3.3,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11375882/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142134542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dry blood spots as a sampling strategy to identify insulin resistance markers during a dietary challenge.","authors":"Stephany Gonçalves Duarte, Carlos M Donado-Pestana, Tushar H More, Larissa Rodrigues, Karsten Hiller, Jarlei Fiamoncini","doi":"10.1186/s12263-024-00752-7","DOIUrl":"10.1186/s12263-024-00752-7","url":null,"abstract":"<p><p>This study aimed to identify markers of postprandial dysglycemia in the blood of self-described healthy individuals using dry blood spots (DBS) as a sampling strategy. A total of 54 volunteers, including 31 women, participated in a dietary challenge. They consumed a high-fat, high-sugar mixed meal and underwent multiple blood sampling over the course of 150 min to track their postprandial responses. Blood glucose levels were monitored with a portable glucometer and individuals were classified into two groups based on the glucose area under the curve (AUC): High-AUC (H-AUC) and Low-AUC (L-AUC). DBS sampling was performed at the same time points as the assessment of glycemia using Whatman 903 Protein Saver filter paper. A gas chromatography-mass spectrometry-based metabolite profiling was conducted in the DBS samples to assess postprandial changes in blood metabolome. Higher concentrations of metabolites associated with insulin resistance were observed in individuals from the H-AUC group, including sugars and sugar-derived products such as fructose and threonic acid, as well as organic acids and fatty acids such as succinate and stearic acid. Several metabolites detected in the GC-MS analysis remained unidentified, indicating that other markers of hyperglycemia remain to be discovered in DBS. Based on these observations, we demonstrated that the use of DBS as a non-invasive and inexpensive sampling tool allows the identification of metabolites markers of dysglycemia in the postprandial period.</p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":"19 1","pages":"18"},"PeriodicalIF":3.3,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11363552/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142114951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effects of Nogo-B deficiency in NAFLD mice and its multiomics analysis of gut microbiology and metabolism.","authors":"Xu Dong, Yu-Ting Xiong, Tingting He, Congyang Zheng, Junjie Li, Yingjie Zhuang, Yingjie Xu, Ye Xiu, Zhixin Wu, Xiaomei Zhao, Xiaohe Xiao, Zhaofang Bai, Lili Gao","doi":"10.1186/s12263-024-00754-5","DOIUrl":"10.1186/s12263-024-00754-5","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Nonalcoholic fatty liver disease (NAFLD) is a prevalent chronic liver ailment that can lead to serious conditions such as cirrhosis and hepatocellular carcinoma. Hepatic Nogo-B regulates glucose and lipid metabolism, and its inhibition has been shown to be protective against metabolic syndrome. Increasing evidence suggests that imbalances in the gut microbiota (GM) and lipid metabolism disorders are significant contributors to NAFLD progression. Nevertheless, it is not yet known whether Nogo-B can affect NAFLD by influencing the gut microbiota and metabolites. Hence, the aim of the present study was to characterize this process and explore its possible underlying mechanisms.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;A NAFLD model was constructed by administering a high-fat diet (HFD) to Nogo-B&lt;sup&gt;-/-&lt;/sup&gt; and WT mice from the same litter, and body weight was measured weekly in each group. The glucose tolerance test (GTT) and insulin tolerance test (ITT) were performed to assess blood glucose levels. At the end of the 12-week period, samples of serum, liver, and intestinal contents were collected and used for serum biochemical marker and inflammatory factor detection; pathology evaluation; and gut microbiome and metabolomics analysis. Spearman's correlation analysis was performed to determine possible correlations between differential gut microbiota and differential serum metabolites between groups.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Nogo-B deficiency attenuated the effects of the HFD, including weight gain, liver weight gain, impaired glucose tolerance, hepatic steatosis, elevated serum lipid biochemicals levels, and liver function. Nogo-B deficiency suppressed M1 polarization and promoted M2 polarization, thus inhibiting inflammatory responses. Furthermore, Nogo-B&lt;sup&gt;-/-&lt;/sup&gt;-HFD-fed mice presented increased gut microbiota richness and diversity, decreased Firmicutes/Bacteroidota (F/B) ratios, and altered serum metabolites compared with those of WT-HFD-fed mice. During analysis, several differential gut microbiota, including Lachnoclostridium, Harryflintia, Odoribacter, UCG-009, and unclassified_f_Butyricoccaceae, were screened between groups. These microbiota were found to be positively correlated with upregulated purine metabolism and bile acid metabolites in Nogo-B deficiency, while they were negatively correlated with downregulated corticosterone and tricarboxylic acid cyclic metabolites in Nogo-B deficiency.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;Nogo-B deficiency delayed NAFLD progression, as demonstrated by reduced hepatocellular lipid accumulation, attenuated inflammation and liver injury, and ameliorated gut microbiota dysbiosis and metabolic disorders. Importantly, Odoribacter was strongly positively correlated with ALB and taurodeoxycholic acid, suggesting that it played a considerable role in the influence of Nogo-B on the progression of NAFLD, a specific feature of NAFLD in Nogo-B&lt;sup&gt;-/-&lt;/sup&gt; mice. The regulatio","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":"19 1","pages":"17"},"PeriodicalIF":3.3,"publicationDate":"2024-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11344411/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142057394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-450a-2-3p targets ERK(1/2) to ameliorate ISO-induced cardiac fibrosis in mice.","authors":"Langsha Liu, Fanyan Luo","doi":"10.1186/s12263-024-00753-6","DOIUrl":"10.1186/s12263-024-00753-6","url":null,"abstract":"<p><strong>Objective: </strong>Cardiac fibrosis is an important contributor to atrial fibrillation (AF). Our aim was to identify biomarkers for AF using bioinformatics methods and explore the regulatory mechanism of miR-450a-2-3p in cardiac fibrosis in mice.</p><p><strong>Methods: </strong>Two datasets, GSE115574 and GSE79768, were obtained from the Gene Expression Omnibus (GEO) database and subsequently merged for further analysis. Differential gene expression analysis was performed to identify differentially expressed genes (DEGs) and miR-450a-2-3p-related differentially expressed genes (MRDEGs). To investigate the underlying mechanism of cardiac fibrosis, a mouse model was established by treating mice with isoproterenol (ISO) and the miR-450a-2-3p agomir.</p><p><strong>Results: </strong>A total of 127 DEGs and 31 MRDEGs were identified and subjected to Gene Ontology (GO) functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis to determine the functions and pathways involved in AF. In the animal model, histological analysis using HE and Masson staining, as well as quantification of the collagen volume fraction (CVF), was performed. The increased expression of α-smooth muscle actin (α-SMA), collagen type I (COL1), collagen type III (COL3), and extracellular signal-regulated kinase 1/2 (ERK(1/2)) at both the transcriptional and translational levels indicated the significant development of myocardial fibrosis in mice induced with isoproterenol (ISO). In addition, the cross-sectional area of cardiomyocytes and the expression of atrial natriuretic peptide (NPPA) and brain natriuretic peptide (NPPB) were increased in the ISO group compared with the control group. However, after overexpression of the miR-450a-2-3p agomir through caudal vein injection, there was a notable improvement in cardiac morphology in the treated group. The expression levels of α-SMA, COL1, COL3, ERK(1/2), NPPA, and NPPB were also significantly decreased.</p><p><strong>Conclusion: </strong>Our study reveals the mechanistic connection between ISO-induced myocardial fibrosis and the miR-450a-2-3p/ERK(1/2) signaling pathway, highlighting its role in the development of cardiac fibrosis. Modulating miR-450a-2-3p expression and inhibiting ERK(1/2) activation are promising approaches for therapeutic intervention in patients with AF.</p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":"19 1","pages":"16"},"PeriodicalIF":3.3,"publicationDate":"2024-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11334388/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142005968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of diet in cancer: the potential of shaping public policy and clinical outcomes in the UK.","authors":"Oliver Britten, Sabrina Tosi","doi":"10.1186/s12263-024-00750-9","DOIUrl":"10.1186/s12263-024-00750-9","url":null,"abstract":"<p><p>Cancer universally represents one of the largest public health concerns, substantially contributing to global disease burden and mortality. The multifaceted interplay of environmental and genetic factors in the disease aetiology and progression has required comprehensive research to elucidate modifiable elements which can reduce the risk of incidence and improve prognosis. Among these factors, diet and nutrition have emerged as the most fundamental with a significant potential for influence and effect. Nutrition is not only an essential part of human survival, but also a vital determinant of overall health. Certain dietary requirements are necessary to support normal physiology. This includes individualised levels of macronutrients (proteins, carbohydrates and fats) and specific micronutrients (vitamins and minerals). Extensive research has demonstrated that diet plays a role in cancer pathogenesis at the genetic, epigenetic and cellular level. Therefore, its potential as a modifiable determinant of cancer pathogenesis for the purpose of prevention and improving management of disease must be further explored and implemented. The ability to influence cancer incidence and outcomes through dietary changes is underutilised in clinical practice and insufficiently recognised among the general public, healthcare professionals and policy-makers. Dietary changes offer the opportunity for autonomy and control over individuals health outcomes. Research has revealed that particular dietary components, as well as cultural behaviours and epidemiological patterns may act as causative or protective factors in cancer development. This review aims to comprehensively synthesise this research to further explore how to best utilise this knowledge within the community and clinical environment for more effective cancer prevention and therapeutic strategies. The identified key areas for improvement include the development of more specific, widely accepted guidelines, promoting increased involvement of dieticians within cancer multidisciplinary teams, enhancing nutritional education for healthcare professionals and exploring the potential implementation of personalised nutrition tools. A greater understanding of the complex interactions between diet and cancer will facilitate informed clinical interventions and public health policies to reduce global cancer burden and improve care for cancer patients and survivors.</p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":"19 1","pages":"15"},"PeriodicalIF":3.3,"publicationDate":"2024-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11298086/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141891041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}